Cerebral amyloid angiopathy (CAA) is almost universally noted in patients with Alzheimer's Disease (AD) (˜90% of individuals) and is commonly found in non-AD elderly individuals (˜30% of those >60 years of age). It is characterized by amyloid-β (Aβ) deposition in cortical cerebral arterioles. CAA is a powerful risk factor for three potentially interrelated diseases: 1) cerebral hemorrhage, 2) ischemic brain injury, and 3) dementia. Though substantial mechanistic and therapeutic progress has been made in preclinical studies (including identification of several interventions that can halt or even reverse CAA formation), progress in the clinic has been very slow. A major reason for this lack of progress has been inadequate methods for accurately diagnosing and quantifying CAA in patients. Definite diagnosis of CAA currently requires brain biopsy, which is rarely clinically indicated. “Possible” or “probable” diagnosis of CAA can be made via Magnetic Resonance Imaging (MRI) utilizing the Boston Criteria, which relies on identification of cortical hemorrhage as an indirect indicator of the presence of CAA. However, this indirect method of diagnosis has many disadvantages, some of which include: 1) it does not quantify CAA severity, 2) it cannot monitor progression of disease over time, 3) it cannot detect CAA prior to onset of cerebral hemorrhage, and 4) it will be unable to monitor response to CAA-directed therapeutics as they become available. Hence, there is a need in the art for a non-invasive compound and method for accurately and selectively diagnosing CAA in humans.